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Event

Anatomy

Negation

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Pain term

Disease term

We have examined an archival series of cases of pancreatic pathology for expression of the EGFR using the anti-EGFR antiserum 12E and found that there is almost ubiquitous overexpression of EGFR in pancreatic cancer and in chronic pancreatitis.

This is in accordance with the data of Ellis et al. [10], in which biopsy specimens of acanthosis nigricans, seborrheic keratoses, and acrochordons showed intense staining for EGF receptors in all epidermal layers, except the stratum corneum, showing that EGFRoverexpression may be one of the concomitant pathognomonic mechanisms responsible for sudden multiple eruption of SK.

Our study, even demonstrating similar expression profiles of EGFR and HER-2 in cancerous and unaffected tissues, confirmed that EGFR is overexpressed in SCC, as compared to ADC samples, whereas HER-2 displays an opposite behaviour [25, 26].

EGFR is overexpressed in about 40% to 80% of NSCLC.28 Downstream signaling by the activated EGFR can be abrogated by small molecule inhibitors, such as erlotinib and gefitinib or by monoclonal antibodies directed towards the extracellular domain of EGFR, such as cetuximab.

In a phase II trial by Kim et al 47 patients with refractory NSCLC or who had diseaserecurrence within 3 months after chemotherapy and tumoroverexpression of EGFR of at least 1+ by IHC received cetuximab with docetaxel (75 mg/m2 iv every 3 weeks).92 Thirteen patients (28%) achieved PR and 8 (17%) had SD.

The proposed development of colorectal cancer evolves from the progressive accumulation of genetic and epigenetic alterations resulting in the transformation of normal colonic mucosa to invasive adenocarcinoma.19 EGFR has been implicated in the initiation of colorectal tumors and has also been noted to be frequently overexpressed in CRC.5,20 The prognostic significance of EGFR in CRC remains unclear.6,20